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Perinatal Asphyxia


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  • 1. Perinatal Asphyxia Dr. Kalpana Malla MD Pediatrics Manipal Teaching HospitalDownload more documents and slide shows on The Medical Post [ ]
  • 2. PERINATAL ASPHYXIADefinition An insult to the fetus or newborn due to lack ofoxygen (hypoxia) and /or lack of perfusion (ischemia) to various organs.Associated with Tissue lactic acidosis • Hypoventilation • Hypercapnea 2
  • 3. PERINATAL ASPHYXIAIncidence1-1.5%20% of perinatal deathsIncreased risk in IDM Toxemic mothers IUGR Breech Postmature 3
  • 4. SEQUENCE OF EVENTS HR…..decrease BP…...decreaseNormal Resp...Rapid breathing….Pr.Apnea….Irreg.breathing…Sec.Apnea Resuscitation Resuscitation Normal Respiration Normal Respiration 4
  • 5. ETIOLOGY 90% Antepartum/ Intrapartum 10% Postpartum FACTORSMaternal:- Hypertension- chronic / pre-eclampsia - Diabetes, anemia,, malnutrition - Hypoxia-Pulmonary/Cardiac/ - heart Ds, Bronchial asthma 5
  • 6. FACTORSMaternal……:HypotensionIntrauterine infectionsProlonged and difficult 2nd stage of labourPlacental: Infarction/fibrosis/abruptionCord Accidents: Prolapse / True knots / compression/Abn. vessels
  • 7. FACTORSFetal:• Infection - intrauterine• Anemia - Feto-fetal or feto maternal transfusion• IUGR/ Postmaturity - Meconium aspiration tracheal plug by blood mucus• Cong malformations - choanal atresia, laryngeal web,D. hernia, TEF,ICH• Hydrops fetalis
  • 8. PATHOPHYSIOLOGYDiving reflex: Shunting of blood to brain ,heart, adrenals andaway from gut, kidney, liver, spleen ,skeletalmuscle and skinProgressive asphyxia: Hypoxia, Hypercapnea, acidosis Pulmonary vasoconstriction, R to L shunt Decrease in HR, CO, BP Cerebral edema- Petechial hemorrhage, SIADH, Na- intracellular accumulation 8
  • 9. TARGET ORGAN-BRAIN HIE:PATHOPHYSIOLOGYHypoxia Alteration in glucose and energymetabolism loss of autoregulation & decreasedcardiac function ischemiaSevere hypoxia and ischemia failure of oxidativephosphorylation & ATP productionAccumulation of Na, Cl,Ca intracellular and K andexcitatory neurotransmitters extracellularneuronal death 9
  • 10. HIE- PATHOLOGY1. Selective neuronal necrosis - Cerebral and cerebellar cortex, Thalamus, brain stemnuclei2. Focal and multifocal cortical necrosis3. Watershed infarct4. Parasagittal cerebral injury5. Periventricular leucomalacia6. Status murmoratus. 10
  • 11. Hypoxic Ischaemic Encephalopathy• Most important consequence of perinatal asphyxia• Hypoxic ischaemic insult to the brain• 25-30% of survivors have permanent damage like CP and MR.• 15-20% with HIE die
  • 12. SARNAT STAGINGFeatures Stage1 Stage 2 Stage3 Mild Moderate Severe1.Level of Hyperalert Lethargic Stuperous consciousness Irritable Obtunded Comatose2.Neuromuscular control. Muscle tone N Hypotonia Flaccid Posture N Flexion Decerebration Reflexes   Decreased / Absent3. Reflexes Suck Weak Weak /Absent Absent Moro Strong Weak Absent 12
  • 13. SARNAT STAGINGFeatures Stagee1 Stage 2 Stage3 Mild Moderate Severe4.Autonomic Gen.sympathetic Gen.Parasymp Both depressed function Pupil Mydriasis Miosis Midposition Resp Spont Spont Periodic,apnea HR Tachycardia bradycardia Variable5.Seizures None common Uncommon6.EEG Normal abnormal abnormal7. Duration <24hr 24hr-14day Day-weeks8.Outcome Good Variable Death
  • 14. SARNAT STAGINGFeatures Stage1(Mild) Stage 2(Moderate) Stage3(Severe)4.Autonomic Gen.sympathetic Gen.Parasymp Both depressed function Pupil Mydriasis Miosis Midposition Resp Spont Spont Periodic,apnea HR Tachycardia bradycardia Variable5.Seizures None common Uncommon6.EEG Normal abnormal abnormal7. Duration <24hr 24hr-14day Day-weeks8.Outcome Good Variable Death
  • 15. APGAR SCORE APGAR Score: 8-10 No asphyxia 5-7 Mild asphyxia 3-4 Moderate asphyxia 0-2 Severe asphyxia Virginia Apgar 0_________ 1__________ 2_____Heart rate 0 <100 >100Respiration 0 weak, irregular good cryReaction 0 slight goodColour blue or pale body pink limbs blue all pinkTone limp some movement active movements limbs well flexed
  • 16. ASSESSMENT/PRECAUTIONSPerinatal1.Awareness of problems and high risk2.Fetal movement count3.Fetal BPP5. Monitor FHR6.Progress of labor7.Fetal scalp -pH8.Presence of meconium 16
  • 17. SYSTEMIC MANIFESTATIONSBrain(28%)- HIE, ICH, Apneic attacks, SeizuresHeart(25%)- PFC, Arrhythmia, Myocardial damage,TR,CCFLungs(23%)- Meconium aspiration, Pul.hemorrhage Pneumothorax, pneumoniaKidney(50%)- Hematuria, ARF, ATN, RVTGIT- NEC, Paralytic ileus 17
  • 18. SYSTEMIC MANIFESTATIONS• Hematologic- DIC, Hyperbilirubinemia, sepsis• Endocrine- SIADH, Adrenal hemorrhage• Metabolic- hypoglycemia, hypocalcemia, hyperbilirubinemia
  • 19. Late effects• Microcephaly• MR• Developmental delay• Cerebral palsy• Epilepsy• Visual, hearing impairement• Behavioral disturbances
  • 20. MANAGEMENT• Ventilation-For hypoxia and hypercapnea• Maintain cerebral perfusion• Correction of hypoglycemia and hypocalcemia• Temperature maintenance• Control of seizure- Anticonvulsants• Cardiac effects-Ionotropes• Renal effects- Dopamine 21
  • 21. CLINICAL MANIFESTATIONS OF NEUROLOGICAL SEQUELAE• Cerebral Palsy- Spastic diplegia, Spastic quadriplegia, Spastic hemiplegia Dystonic Choreo athetotic• Mental retardation• Epilepsy• Auditory, visual and language difficulties 22
  • 22. PROGNOSIS• Overall mortality - 10-20%• Neurological sequele - 20-45%• Sarnat Stages 1- 100% Normal neurological outcome 2- 80% Normal neurological outcome 3- 50% deaths, 50% major neurological sequelae• Risk for CP - 5-10%• Subtle school problems in neurologically and mentally normal survivors of HIE stage 1-nil, stage 2- 18-35% 23
  • 23. Thank youDownload more documents and slide shows on The Medical Post [ ]